权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Engineering Approach to the Ventilatory Pump

呼吸泵的工程方法

基本信息

批准号：
7256228
负责人：
Aladin M Boriek
金额：
$ 32.11万
依托单位：
BAYLOR COLLEGE OF MEDICINE
依托单位国家：
美国
项目类别：
财政年份：
2004
资助国家：
美国
起止时间：
2004-08-01 至 2009-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7256228
关键词：
Breathing Canis familiaris Cause of Death Chest wall structure Chronic Chronic Obstructive Airway Disease Clinical Complement Condition Data Disease Electron Beam Tomography Engineering Evaluation Failure Fluoroscopy Frequencies Goals Health Human Individual Knowledge Lung Lung diseases Lung volume reduction surgery Measures Mechanics Mediating Membrane Modeling Morbidity - disease rate Motion Muscle Muscle Contraction Muscle Fibers Muscle function Operative Surgical Procedures Patients Property Publishing Pulmonary Emphysema Pump Rate Relative (related person)Respiratory Diaphragm Respiratory Failure Scanning Shapes Slice Speed Staging Stress Structural Models Structure Techniques Testing Total Lung Capacity base cost expiration functional restoration human subject improved in vivo interest kinematics lung volume mathematical model membrane model mortality pressure productivity loss programs respiratory rib bone structure theories

项目摘要

DESCRIPTION (provided by applicant): Respiratory failure is a major cause of morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD). However, the mechanical determinants of ventilatory pump function are still not well understood. Our goal is to use an engineering approach to investigate the mechanical factors that mediate pump failure in COPD. Hyperinflation of the lungs and extreme diaphragm shortening can distort the sheet of the diaphragm, cause loss of its membrane curvature, and reduce its muscle force. This will severely limit the function of the ventilatory pump. Our objective is to build a general model of diaphragm mechanics that can be utilized to evaluate the effect of lung volume reduction surgery on respiratory pump function in patients with severe emphysema. We will extend our knowledge of diaphragm and chest wall mechanics in dogs, and will begin to apply the same principles and approaches to the study of ventilatory mechanics in normal human subjects and patients with severe emphysema before and after lung volume reduction surgery (LVRS). Finally, we will develop a comprehensive theory of diaphragm mechanics that can eventually be used to predict diaphragm muscle function in both healthy and diseased states. We will achieve this objective with in vivo studies of diaphragm mechanics in dogs and humans complemented with mathematical modeling techniques. Our specific aims are: Specific Aim #1: To determine how hyperinflation of the lungs alters the pressure generating ability of the diaphragm during simultaneous sub-maximal and maximal activation of both hemi-diaphragms. Hypothesis 1: Extreme muscle contraction of both hemi-diaphragms at high frequencies of stimulation and at lower lung volumes causes flattening and distortion of the membrane of the diaphragm, and therefore its generating ability of pressure is severely compromised. Specific Aim #2: To develop a comprehensive mechanical model of the diaphragm. Hypothesis 3: A comprehensive mechanical model of the diaphragm that utilizes both structure and constitutive relationships of the diaphragm should provide sufficient quantitative information on the evaluation of the pressure generating ability of the ventilatory pump. Specific Aim #3: To evaluate diaphragm function in patients with end-stage emphysema before and after LVRS, and in normal humans. Hypothesis 2a: In normal individuals, muscle fibers are oriented along the direction of maximum principal curvature, Hypothesis 2b: In severe emphysema patients, the diaphragm is comparatively flattened, and after LVRS, there is a gain in diaphragm muscle fiber curvature. Therefore, membrane tension is transmitted into trans-diaphragmatic pressure more effectively than before the surgery. Once we obtained the distribution of principal curvatures we will use our model of diaphragm mechanics developed in Aim 2 to predict diaphragm function in normal individuals and patients with severe emphysema before and after LVRS. The completion of these aims will significantly enhance our fundamental understanding of the ventilatory pump function in health and disease.

描述（由申请人提供）：呼吸衰竭是慢性阻塞性肺病（COPD）患者发病和死亡的主要原因。然而，通气泵功能的机械决定因素仍不清楚。我们的目标是使用工程方法来研究导致慢性阻塞性肺病（COPD）泵故障的机械因素。肺部过度充气和膈肌极度缩短会使膈膜变形，导致其膜曲率丧失，并降低其肌肉力量。这将严重限制通气泵的功能。我们的目标是建立一个膈肌力学的通用模型，可用于评估肺减容手术对严重肺气肿患者呼吸泵功能的影响。我们将扩展我们对狗的膈肌和胸壁力学的了解，并将开始应用相同的原理和方法来研究正常人类受试者和严重肺气肿患者在肺减容手术（LVRS）前后的通气力学。最后，我们将开发一种全面的膈肌力学理论，最终可用于预测健康和疾病状态下的膈肌功能。我们将通过对狗和人类隔膜力学的体内研究并辅以数学建模技术来实现这一目标。我们的具体目标是：具体目标#1：确定在两个半隔膜同时次最大和最大激活期间，肺部过度充气如何改变隔膜的压力产生能力。假设1：在高频率的刺激和较低的肺容量下，两侧膈肌的极度肌肉收缩导致膈膜变平和扭曲，因此其产生压力的能力受到严重损害。具体目标#2：开发隔膜的综合机械模型。假设3：利用隔膜结构和本构关系的隔膜综合力学模型应该为呼吸泵压力产生能力的评估提供足够的定量信息。具体目标#3：评估 LVRS 前后终末期肺气肿患者以及正常人的膈肌功能。假设2a：正常个体肌纤维沿最大主曲率方向取向。假设2b：严重肺气肿患者膈肌相对扁平，LVRS 后膈肌纤维曲率有所增加。因此，膜张力比手术前更有效地传递为跨膈压力。一旦我们获得主曲率分布，我们将使用目标 2 中开发的膈肌力学模型来预测 LVRS 前后正常个体和严重肺气肿患者的膈肌功能。这些目标的完成将显着增强我们对通气泵在健康和疾病中的功能的基本理解。